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Microbiota and IL-33/31 Axis Linkage: Implications and Therapeutic Perspectives in Atopic Dermatitis and Psoriasis
Laura Bonzano1, Francesco Borgia2, Rossella Casella3
1Dermatology Unit, Azienda Unità Sanitaria Locale-IRCCS di Reggio Emilia, 42122 Reggio Emilia, Italy.
Abstract:
Microbiome dysbiosis and cytokine alternations are key features of atopic dermatitis (AD) and psoriasis (PsO), two of the most prevalent and burdensome pruritic skin conditions worldwide. Interleukin (IL)-33 and IL-31 have been recognized to be major players who act synergistically in the pathogenesis and maintenance of different chronic inflammatory conditions and pruritic skin disorders, including AD and PsO, and their potential role as therapeutic targets is being thoroughly investigated. The bidirectional interplay between dysbiosis and immunological changes has been extensively studied, but there is still debate regarding which of these two factors is the actual causative culprit behind the aetiopathological process that ultimately leads to AD and PsO. We conducted a literature review on the Pubmed database assessing articles of immunology, dermatology, microbiology and allergology with the aim to strengthen the hypothesis that dysbiosis is at the origin of the IL-33/IL-31 dysregulation that contributes to the pathogenesis of AD and PsO. Finally, we discussed the therapeutic options currently in development for the treatment of these skin conditions targeting IL-31, IL-33 and/or the microbiome.
Insights
Microbiome dysbiosis may initiate the immune imbalance seen in atopic dermatitis (AD) and psoriasis (PsO), driving interleukin-33 (IL-33) and IL-31 related inflammation. This suggests microbiome-targeted therapies could treat these chronic skin conditions.
Area of Science:
- Immunology
- Dermatology
- Microbiology
- Allergology
Background:
- Atopic dermatitis (AD) and psoriasis (PsO) are common, burdensome pruritic skin diseases characterized by microbiome dysbiosis and altered cytokine profiles.
- Interleukin-33 (IL-33) and IL-31 are key cytokines implicated in the pathogenesis and maintenance of chronic inflammatory skin conditions like AD and PsO.
- The interplay between dysbiosis and immune dysregulation in AD and PsO is complex, with ongoing debate about the primary causative factor.
Purpose of the Study:
- To investigate the hypothesis that microbiome dysbiosis is the initiating factor in the IL-33/IL-31 dysregulation observed in AD and PsO.
- To review existing literature on the roles of microbiome, IL-33, and IL-31 in the pathogenesis of these skin conditions.
Main Methods:
- A literature review was conducted using the PubMed database.
- Articles from immunology, dermatology, microbiology, and allergology fields were assessed.
Main Results:
- The review supports the hypothesis that dysbiosis precedes and potentially drives the IL-33/IL-31 axis dysregulation in AD and PsO.
- Evidence suggests a significant link between microbial imbalances and the inflammatory pathways involved in these conditions.
Conclusions:
- Microbiome dysbiosis is proposed as a potential root cause for the IL-33/IL-31 dysregulation contributing to atopic dermatitis and psoriasis.
- Therapeutic strategies targeting the microbiome, IL-31, and IL-33 are under development for managing these pruritic skin disorders.
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